Pulmonary and Extrapulmonary Effects of Increased Colloid Osmotic Pressure During Endotoxemia in Rats: Pulmonary edema

Guyton and Lindsey demonstrated that when plasma COP was reduced by half, the threshold hydrostatic pressure necessary for the formation of pulmonary edema fell from 25 to 13 mm Hg. An increase in the hydrostatic pressure above a threshold appears to be a prerequisite for edema formation. When capillary permeability is increased, the transvascular oncotic pressure gradient is decreased. In this setting, the hydrostatic pressure will be the major determinant of pulmonary edema, rather than oncotic pressure. The MABP in our endotoxemic rat model was decreased by 20% (Fig 5) at 4 h following endotoxin infusion. It is possible that increased capillary permeability may decrease the hydrostatic pressure threshold for pulmonary dysfunction. Reduced plasma COP with normal permeability, however, can decrease the hydrostatic pressure threshold, which is necessary for edema formation.
Ernest et al showed that, in septic patients, saline solution infusion increased extracellular fluid volume by approximately the volume infused and the infusion of 5% albumin increased extracellular fluid volume by double the volume infused, indicating fluid movement from the intracellular space to extracellular space. We speculate that in our rat model albumin infusion increased intravascular fluid volume by shifting fluid from the intracellular compartment. This scenario, in endotoxin-albumin-treated rats, may result in increased capillary hydrostatic pressure and increased extravasation of fluid from the vascular compartment, when compared to endo-toxemic rats that were not treated with albumin. In fact, the MABP was consistently higher in endotoxinalbumin-treated rats than in endotoxemic rats (Fig 5). Whether increased capillary hydrostatic pressure in this rat model is ultimately responsible for a larger pulmonary edema formation warrants investigation. canadian health&care mall